Department of Mechanical Engineering and Materials Science, Washington University in St. Louis. St. Louis, MO, 63130, United States; Center of Regenerative Medicine, Washington University in St. Louis. St. Louis, MO, 63130, United States; Department of Materials Science and Engineering, Ohio State University. Columbus, OH, 43210, United States.
Department of Mechanical Engineering and Materials Science, Washington University in St. Louis. St. Louis, MO, 63130, United States; Institute of Materials Science and Engineering, Washington University in St. Louis. St. Louis, MO, 63130, United States.
Acta Biomater. 2022 Apr 15;143:295-309. doi: 10.1016/j.actbio.2022.03.021. Epub 2022 Mar 14.
Vascularization of the poorly vascularized limbs affected by critical limb ischemia (CLI) is necessary to salvage the limbs and avoid amputation. Effective vascularization requires forming not only capillaries, but also arterioles and vessel branching. These processes rely on the survival, migration and morphogenesis of endothelial cells in the ischemic limbs. Yet endothelial cell functions are impaired by the upregulated TGFβ. Herein, we developed an injectable hydrogel-based drug release system capable of delivering both VEGF and Dll4 to synergistically restore endothelial cellular functions, leading to accelerated formation of capillaries, arterioles and vessel branching. In vitro, the Dll4 and VEGF synergistically promoted the human arterial endothelial cell (HAEC) survival, migration, and formation of filopodial structure, lumens, and branches under the elevated TGFβ1 condition mimicking that of the ischemic limbs. The synergistic effect was resulted from activating VEGFR2, Notch-1 and Erk1/2 signaling pathways. After delivering the Dll4 and VEGF via an injectable and thermosensitive hydrogel to the ischemic mouse hindlimbs, 95% of blood perfusion was restored at day 14, significantly higher than delivery of Dll4 or VEGF only. The released Dll4 and VEGF significantly increased density of capillaries and arterioles, vessel branching point density, and proliferating cell density. Besides, the delivery of Dll4 and VEGF stimulated skeletal muscle regeneration and improved muscle function. Overall, the developed hydrogel-based Dll4 and VEGF delivery system promoted ischemic limb vascularization and muscle regeneration. STATEMENT OF SIGNIFICANCE: Effective vascularization of the poorly vascularized limbs affected by critical limb ischemia (CLI) requires forming not only capillaries, but also arterioles and vessel branching. These processes rely on the survival, migration and morphogenesis of endothelial cells. Yet endothelial cell functions are impaired by the upregulated TGFβ in the ischemic limbs. Herein, we developed an injectable hydrogel-based drug release system capable of delivering both VEGF and Dll4 to synergistically restore endothelial cell functions, leading to accelerated formation of capillaries, arterioles and vessel branching.
受严重肢体缺血(CLI)影响的肢体血供不足,需要进行血管化治疗以挽救肢体并避免截肢。有效的血管化不仅需要形成毛细血管,还需要形成小动脉和血管分支。这些过程依赖于缺血肢体中内皮细胞的存活、迁移和形态发生。然而,内皮细胞功能受到缺血肢体中上调的 TGFβ 的损害。在此,我们开发了一种可注射水凝胶药物释放系统,能够同时递送 VEGF 和 Dll4,以协同恢复内皮细胞功能,加速毛细血管、小动脉和血管分支的形成。在体外,Dll4 和 VEGF 在模拟缺血肢体的 TGFβ1 升高条件下,协同促进人动脉内皮细胞(HAEC)的存活、迁移和形成丝状伪足结构、管腔和分支。协同作用是通过激活 VEGFR2、Notch-1 和 Erk1/2 信号通路实现的。通过向缺血小鼠后肢注射和热敏水凝胶递送来 Dll4 和 VEGF 后,第 14 天恢复了 95%的血流灌注,明显高于仅递送 Dll4 或 VEGF。释放的 Dll4 和 VEGF 显著增加了毛细血管和小动脉密度、血管分支点密度和增殖细胞密度。此外,Dll4 和 VEGF 的递送刺激了骨骼肌再生并改善了肌肉功能。总体而言,所开发的基于水凝胶的 Dll4 和 VEGF 递送系统促进了缺血肢体的血管化和肌肉再生。